Experiments on the nature of virulence of group A streptococci and on the means by which streptococci produce glomerulonephritis are continuing. Investigations continue into the distribution and function of contractile proteins of smooth muscle type. Experiments are in progress on the pathogenesis and ultrastructure of atherosclerosis induced by the synergy of immunological injury and lipid-rich diet. We are also attempting to cause regression of such atherosclerosis by dietary modification. A detailed comparative histologic study is being carried out of the coronary arteries of many rejected human cardiac homografts and rabbit coronary arteries exhibiting atherosclerosis induced by the synergy of immunological injury and lipid-rich diet. Ultrastructural studies are being carried out on the changes in the coronary arteries of rejected rabbit cardiac homografts.